prl expression Search Results


90
Sino Biological plasmid encoding prolactin prl
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
Plasmid Encoding Prolactin Prl, supplied by Sino Biological, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Promega 0.05 mg prl-cmv plasmid expressing renilla luciferase
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
0.05 Mg Prl Cmv Plasmid Expressing Renilla Luciferase, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Promega gli-responsive and renilla luciferase expression vectors prl-cmv
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
Gli Responsive And Renilla Luciferase Expression Vectors Prl Cmv, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Promega the prl-null luciferase protein expression plasmid
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
The Prl Null Luciferase Protein Expression Plasmid, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Qiagen prl-3 chimeric mab
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
Prl 3 Chimeric Mab, supplied by Qiagen, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Promega prl-tk dual-luciferase mirna target expression vector
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
Prl Tk Dual Luciferase Mirna Target Expression Vector, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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90
Promega 50 ng of renilla-expressing vector prl-tk luc
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
50 Ng Of Renilla Expressing Vector Prl Tk Luc, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Promega prl-tk expression
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
Prl Tk Expression, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Promega prl-tkluc construct, which expresses renilla luciferase and is driven by the herpes simplex virus thymidine kinase (tk) promoter
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
Prl Tkluc Construct, Which Expresses Renilla Luciferase And Is Driven By The Herpes Simplex Virus Thymidine Kinase (Tk) Promoter, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/prl-tkluc construct, which expresses renilla luciferase and is driven by the herpes simplex virus thymidine kinase (tk) promoter/product/Promega
Average 90 stars, based on 1 article reviews
prl-tkluc construct, which expresses renilla luciferase and is driven by the herpes simplex virus thymidine kinase (tk) promoter - by Bioz Stars, 2026-04
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90
Promega constitutively expressed renilla luciferase reporter prl-cmv
A. Schematic <t>showing</t> <t>ACE2</t> tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin <t>(PRL)</t> under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.
Constitutively Expressed Renilla Luciferase Reporter Prl Cmv, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Promega prl-tk-luc that constitutively expresses renilla luciferase from the thymidine kinase promoter
A . ARPE-19 cells in serum free medium were treated with R9-SOCS3-KIR or the control peptide (20 μM) for 1 hr followed by treatment with C5a (50 ng/ml) for 4 hr. They were then co-transfected with a mixture of plasmids with NF-kB promoter driven <t>firefly</t> <t>luciferase</t> and another plasmid with thymidine kinase driven <t>Renilla</t> luciferase as an internal control and grown for 24 hrs in 1% FBS containing medium. Cell lysates, were harvested and used to measure relative luciferase units using a Dual luciferase kit from Promega. **, p = 0.001. Error bars indicae the standard deviation. Abbrev: K, R9-SOCS3-KIR, Ctrl: R9-SOCS3-KIR-scrambled peptide. B. R9-SOCS3-KIR suppressed C5a-induced nuclear translocation of NF-κB subunit p65. ARPE-19 cells were grown overnight in 8 well plates, placed in serum-free medium and treated with R9-SOCS3-KIR or its control peptide at 20 μM for 1 hr, followed by addition of C5a (50 ng/ml) for 30 min. Cells were stained with an antibody to p65, followed by staining with Cy-3 conjugated secondary antibody and DAPI, and imaged in a fluorescence microscope using the same exposure time and light intensity. Scale bars equal 50 μm.
Prl Tk Luc That Constitutively Expresses Renilla Luciferase From The Thymidine Kinase Promoter, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Inserm Transfert expression vectors for rat prl receptor long and short forms
A . ARPE-19 cells in serum free medium were treated with R9-SOCS3-KIR or the control peptide (20 μM) for 1 hr followed by treatment with C5a (50 ng/ml) for 4 hr. They were then co-transfected with a mixture of plasmids with NF-kB promoter driven <t>firefly</t> <t>luciferase</t> and another plasmid with thymidine kinase driven <t>Renilla</t> luciferase as an internal control and grown for 24 hrs in 1% FBS containing medium. Cell lysates, were harvested and used to measure relative luciferase units using a Dual luciferase kit from Promega. **, p = 0.001. Error bars indicae the standard deviation. Abbrev: K, R9-SOCS3-KIR, Ctrl: R9-SOCS3-KIR-scrambled peptide. B. R9-SOCS3-KIR suppressed C5a-induced nuclear translocation of NF-κB subunit p65. ARPE-19 cells were grown overnight in 8 well plates, placed in serum-free medium and treated with R9-SOCS3-KIR or its control peptide at 20 μM for 1 hr, followed by addition of C5a (50 ng/ml) for 30 min. Cells were stained with an antibody to p65, followed by staining with Cy-3 conjugated secondary antibody and DAPI, and imaged in a fluorescence microscope using the same exposure time and light intensity. Scale bars equal 50 μm.
Expression Vectors For Rat Prl Receptor Long And Short Forms, supplied by Inserm Transfert, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


A. Schematic showing ACE2 tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin (PRL) under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.

Journal: bioRxiv

Article Title: The hyperlipidaemic drug fenofibrate significantly reduces infection by SARS-CoV-2 in cell culture models

doi: 10.1101/2021.01.10.426114

Figure Lengend Snippet: A. Schematic showing ACE2 tagged with LgBIT and SmBIT. B. HEK-293 cells were transfected with combinations of plasmids encoding LgBIT or SmBIT fused to either protein kinase A regulatory subunit (PRKAR2) or catalytic subunit (PRKACA), ATG5 or ACE2. The results (mean ± S.D., n = 5) were normalized to the luminescence measured in cells transfected with protein kinase A reporters (positive control). C. HEK-293 cells were transfected with plasmids encoding ACE2 nanoBIT reporters under the control of the HSV TK promoter and ACE2 or prolactin (PRL) under the control of the CMV promoter. The results (mean ± S.D., n = 4) were normalized to the luminescence measured in cells transfected with protein kinase A reporters and prolactin. D. HEK-293 cells were transfected with NanoBIT-tagged ACE2 reporters and incubated with sodium valproate or clofibrate at a concentration equal to 1x, 2x or 3x the reported C max of the drug. After 1 hour, luminescence was measured and normalized (mean ± S.D., n =4) to that measured in cells treated with DMSO. E. A series of other fibrates were similarly evaluated in the assay. The luminescence measured (mean ± S.D., n = 5-11, solid bars) was significantly different to that measured in cells treated with solvent where shown. When these fibrates were incubated with purified LgBIT and HiBIT-RBD to create a constitutively active nanoluc, each of these fibrates were found to inhibit nanoluciferase (bezafibrate 35 ± 7 %, ciprofibrate 55 ± 6 %, fenofibric acid 46 ± 3 %, fenofibrate 69 ± 5 %, gemfibrozil 61 ± 2 % of the activity measured in the presence of DMSO). To correct for this, the luminescence measurements from cells treated with fibrates in cells were divided by these latter values to estimate the effect of the drugs on dimerization (hatched bars). Significant difference from control is shown as *, P < 0.05; **, P < 0.01; ***, P < 0.005.

Article Snippet: The plasmid pcDNA3 encoding ACE2 was obtained from GenScript (OHu20260); the plasmid encoding prolactin (PRL) was obtained from Sino Biological (HG10275-CY).

Techniques: Transfection, Positive Control, Incubation, Concentration Assay, Purification, Activity Assay

A . ARPE-19 cells in serum free medium were treated with R9-SOCS3-KIR or the control peptide (20 μM) for 1 hr followed by treatment with C5a (50 ng/ml) for 4 hr. They were then co-transfected with a mixture of plasmids with NF-kB promoter driven firefly luciferase and another plasmid with thymidine kinase driven Renilla luciferase as an internal control and grown for 24 hrs in 1% FBS containing medium. Cell lysates, were harvested and used to measure relative luciferase units using a Dual luciferase kit from Promega. **, p = 0.001. Error bars indicae the standard deviation. Abbrev: K, R9-SOCS3-KIR, Ctrl: R9-SOCS3-KIR-scrambled peptide. B. R9-SOCS3-KIR suppressed C5a-induced nuclear translocation of NF-κB subunit p65. ARPE-19 cells were grown overnight in 8 well plates, placed in serum-free medium and treated with R9-SOCS3-KIR or its control peptide at 20 μM for 1 hr, followed by addition of C5a (50 ng/ml) for 30 min. Cells were stained with an antibody to p65, followed by staining with Cy-3 conjugated secondary antibody and DAPI, and imaged in a fluorescence microscope using the same exposure time and light intensity. Scale bars equal 50 μm.

Journal: bioRxiv

Article Title: Suppressor of Cytokine Signaling 3 Derived Peptide as a Therapeutic for Inflammatory, and Oxidative Stress Induced Damage to the Retina

doi: 10.1101/2023.09.04.556227

Figure Lengend Snippet: A . ARPE-19 cells in serum free medium were treated with R9-SOCS3-KIR or the control peptide (20 μM) for 1 hr followed by treatment with C5a (50 ng/ml) for 4 hr. They were then co-transfected with a mixture of plasmids with NF-kB promoter driven firefly luciferase and another plasmid with thymidine kinase driven Renilla luciferase as an internal control and grown for 24 hrs in 1% FBS containing medium. Cell lysates, were harvested and used to measure relative luciferase units using a Dual luciferase kit from Promega. **, p = 0.001. Error bars indicae the standard deviation. Abbrev: K, R9-SOCS3-KIR, Ctrl: R9-SOCS3-KIR-scrambled peptide. B. R9-SOCS3-KIR suppressed C5a-induced nuclear translocation of NF-κB subunit p65. ARPE-19 cells were grown overnight in 8 well plates, placed in serum-free medium and treated with R9-SOCS3-KIR or its control peptide at 20 μM for 1 hr, followed by addition of C5a (50 ng/ml) for 30 min. Cells were stained with an antibody to p65, followed by staining with Cy-3 conjugated secondary antibody and DAPI, and imaged in a fluorescence microscope using the same exposure time and light intensity. Scale bars equal 50 μm.

Article Snippet: The plasmid, pNF-kB-Luc that has the NF-kB promoter linked to firefly luciferase and a plasmid that constitutively expresses Renilla luciferase from the thymidine kinase promoter (pRL-TK-Luc) were purchased from Promega (Madison, WI). pRL-TK-Luc serves as an internal control to test the efficiency of transfection.

Techniques: Transfection, Luciferase, Plasmid Preparation, Standard Deviation, Translocation Assay, Staining, Fluorescence, Microscopy